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      Fundamental differences in the dynamics of CNS lesion development and composition in MP4- and MOG peptide 35-55-induced experimental autoimmune encephalomyelitis.

      Clinical Immunology (Orlando, Fla.)
      Animals, B-Lymphocytes, physiology, Brain, pathology, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental, immunology, Female, Glycoproteins, Mice, Mice, Inbred C57BL, Multiple Sclerosis, Myelin Basic Protein, Myelin Proteolipid Protein, Myelin-Oligodendrocyte Glycoprotein, Peptide Fragments, Recombinant Fusion Proteins, Spinal Cord

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          Abstract

          Multiple sclerosis (MS) is characterized by a dynamic inflammatory process in which CNS lesions of distinct cellular composition coexist. In particular the formation of B cell plaques has been ascribed an important role as predictor of disease progression. Here we show that the novel MBP-PLP fusion protein (MP4)-induced experimental autoimmune encephalomyelitis (EAE) of C57BL/6 mice fulfils these criteria inducing differential cellular infiltration of B cells, T cells, macrophages and granulocytes and permitting the quantification and staging of the disease. On the contrary, both key features - dynamic CNS inflammation and B cell infiltration - were absent in the classical MOG:35-55-induced EAE of C57BL/6 mice, which was characterized by a static CD4(+) T cell and macrophage-mediated CNS immunopathology throughout the disease. MP4-induced EAE may thus provide a unique opportunity for studying immune-pathomechanisms of the disease that have been previously neglected due to experimental shortcomings in murine EAE.

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